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Biomedical subjects

S Teichberg

Publications and source records attributed to S Teichberg.

At least 91 records · Page 5Linked to original sources
PubMed1981

Electron microscope cytochemical analysis of chronic myelocytic leukemia: a case report.

A patient with Philadelphia chromosome positive CML was studied to characterize the blast transformation. Peripheral blood and bone marrow at the onset of the blast crisis were evaluated with cytochemistry, chromosome analysis, cell surface markers, terminal transferase assay, and electron microscopy. Although light microscopic examination and cytochemistry suggested lymphoblastic morphology, ultrastructural cytochemistry demonstrated the myelomonocytic features of the transformation. This study suggests that electron microscopic cytochemistry is useful in evaluating the heterogeneous nature of the blast phase of CML.

Adult↗
PubMed1981

Jejunal macromolecular absorption and bile salt deconjugation in protein-energy malnourished rats.

The combined stress of protein-energy malnutrition (PEM) and exposure of the jejunum to pathophysiological (0.5 mM) levels of a bacterial metabolite, deconjugated bile salts, led to alterations not apparent with either stress alone. Perfusion of the jejunum of PEM rats with 0.5 mM deoxycholate (DCh) and a 40,000 dalton macromolecular tracer, horseradish peroxidase, led to higher serum horseradish peroxidase levels than were seen in PEM rats not exposed to DCh or in well-nourished controls treated with DCh. Semiquantitative cytochemical analysis indicated an increased number of villi with horseradish peroxidase penetration in PEM rats treated with 0.5 mM DCh. DCh perfusion of PEM rats also produced fine structural damage to epithelial cells not apparent in other preparations. And, perfusion with 0.5 mM cholate only produced sodium secretion in PEM rats. These observations in an animal model of PEM suggest that malnourished children with a colonic type of bacterial overgrowth of the small bowel may attain increased levels of foreign antigens or toxins from the intestinal lumen.

Animals↗
PubMed1981

Does treatment of hypertension prevent renal failure?

The association between malignant hypertension and renal insufficiency is now well established. The previous adage of not treating this entity for fear of precipitating renal failure has now been replaced by one of aggressive medical therapy as a means to prevent further renal damage. Even when treatment appears to cause renal insufficiency, continued aggressive therapy is indicated as the majority of these people will either stabilize or even improve their renal function. The association of renal failure and benign hypertension is less clear. We feel that if long-term controlled studies could be performed, benefit would be evident. However, even without this evidence, the ability to prevent the malignant hypertensive lesion is sufficient reason to aggressively treat this group.

Animals↗
PubMed1981

Bile salt-enhanced rat jejunal absorption of a macromolecular tracer.

Bile salt deconjugation may occur in the jejunum under conditions of fecal colonic overgrowth of the small intestine. We studied the effects of conjugated and deconjugated bile salts on rat jejunal absorption of a macromolecular tracer, horseradish peroxidase, in an in vivo perfusion system. At a 0.5 mM perfusion concentration, only the deconjugated bile salts, cholate and deoxycholate, produced a significant increase in horseradish peroxidase absorption into serum. At a 0.5 mM concentration of the conjugated salt, taurocholate, horseradish peroxidase-absorption was indistinguishable from that seen in bile salt-free preparations. At a higher 5 mM concentration, both the conjugated and deconjugated salts increased jejunal HRP absorption into serum over that seen in bile salt-free preparations; this absorption wa most marked with the deconjugated salts. At a 0.5 mM level, the bile salts induced minimal sodium and glucose transport alterations but did not produce evidence of morphologic damage to villi or absorptive epithelial cell organelles. At a 5 mM level, the deconjugated salts induced glucose and sodium transport abnormalities and appeared to damage cellular organelles. Our observations suggest that an alteration in the tight junctional barrier to macromolecular absorption may play a role in some of the enhanced horseradish peroxidase absorption seen with deoxycholic acid in these experiments. The process of an increased absorption of intact macromolecules induced by products of bacterial metabolism may be of pathologic significance in the etiology of immunologically related intestinal disease or in toxigenic processes.

Animals↗
PubMed1980

The effects of phenobarbital and diphenylhydantoin on liver function and morphology.

Sixty-three children with seizure disorders receiving phenobarbital and/or diphenylhydantoin for more than 12 months had liver function tests evaluated. All 56 whose serum anticonvulsant concentrations were in the therapeutic range had elevations of their serum gamma glutamyl transpeptidase activity. Of the 11 who had elevated SGOT and SGPT concentrations initially, six had persistent transaminase abnormalities for more than 20 weeks. Liver tissue from these six patients revealed by light microscopy uniform swelling of the hepatocytes without cell necrosis, inflammation, fibrosis, or disturbance of hepatic architecture. Electron microscopy demonstrated proliferation of the smooth endoplasmic reticulum without other ultrastructural alterations. All six patients were maintained on the same dosages of PB and/or DPH, and their transaminase activities returned to normal within eight to 14 months. The clinical well being of these patients, the transient nature of their SGOT and SGPT elevations, and the absence of specific histopathology suggest that chronic treatment with PB and/or DPH does not result in hepatotoxicity but rather in enzyme induction. The data indicate that liver biopsies are not warranted in such children and that PB and DPH may be continued despite mild elevations of SGOT and SGPT, without concern for hepatic damage.

Adolescent↗
PubMed1979

Alterations of intestinal and renal functions in rats after intraperitoneal injections of lead acetate.

When lead acetate was administered intraperitoneally to young rats at a dose of 20 mg/kg (five times a week for 6 weeks), their growth rate was retarded when compared with controls injected with sodium acetate. Only a small amount of the heavy metal reached the circulation and exerted limited effects on typical target organs. However, large, electron-dense inclusion bodies were found in the abdominal cavity. The in vivo intestinal absorption of glucose was reduced. When perfused at 40 mM concentration, the experimental animals had a mean absorption rate of 152.1 nmol/min . cm vs. 230.6 in the controls (p less than 0.01). Also, sodium and potassium transport was reduced. No effects were observed on amino acid transport and (Na+-K+)-ATPase. Mg++-ATPase, glucose-6-phosphatase, fructose-1, 6-diphosphatase, pyruvate kinase, succinic dehydrogenase, and tryptophan hydroxylase in the small intestinal mucosa and the kidney were unaltered. Renal alkaline phosphatase was decreased. These studies confirm the greater susceptibility of some active transport mechanisms of the small intestinal mucosa to lead toxicity, compared to those of the kidney.

Amino Acids↗
PubMed1978

Response of rat intestine to a hyperosmotic feeding.

After a single force-feeding of hypertonic (1300 mOsm) mannitol to rats there is rapid osmotic equilibration of the jejunal fluid, a sharp drop in luminal mannitol concentration and large influxes of water and sodium. During osmotic equilibration there was a significant loss of cells from the jejunal mucosa. In hypertonically fed rats there was an accumulation of protein, DNA, [3H]thymidine-labeled DNA, and disaccharidases in intestinal washings. Brush border disaccharidase specific activities on the jejunal mucosa were unaltered. Under the light microscope jejunal villi from hypertonic mannitol rats were comparable to controls. Some epithelial cells from rats force-fed hypertonic mannitol showed transient ultrastructural damage. Microvilli of some cells were shortened and fused at their bases 20 and 40 min after the force-feeding. By 120 min epithelial cell microvilli were all normal in appearance. In hypertonically fed rats the lateral interdigitating plasma membranes became disorganized. Large fragments budded off into one cell and fused to form larger stuctures. By 120 min many lysosomal autophagic vacuoles and residual bodies were seen. A single hypertonic force feeding produced jejunal cell loss associated with loss of brush border disaccharidases and focal ultrastructural damage.

Animals↗
PubMed1978

Alterations in rat jejunal permeability to a macromolecular tracer during a hyperosmotic load.

The effects of intraluminal hyperosmolality on the intestinal permeability of a macromolecular tracer, horseradish peroxidase, was assessed in rats by light and electron microscopic cytochemistry. After 60 minutes of an intraluminal hypertonic perfusion of 600 mOsM mannitol, horseradish peroxidase was demonstrable in the intercellular spaces between adjacent absorptive epithelial cells of jejunal villi, along the microvillar brush border, in numerous pinocytotic vesicles, in multivesicular bodies, as well as in large lysosomes. Horseradish peroxidase was frequently found extending from the luminal surface of the cell through the tight junctional region and into more basal portions of the intercellular space. In occasional cells, fragments of the interdigitating plasma membranes of two adjacent absorptive cells appeared to bud off into the cytoplasm of one cell. In contrast, after 60 minutes of isotonic perfusion, horseradish peroxidase was confined to the microvillar brush border, a few pinocytotic vesicles, and occasional multivesicular bodies. These experiments suggest that the passage of macromolecules across the jejunal epithelium of adult rats is enhanced under conditions of luminal hyperosmotic stress. This may be due to an alteration in the functional integrity of the tight junctional macromolecular barrier or to an enhanced rate of pinocytosis.

Animals↗
PubMed1978

Experimental acute hypothermia and intestinal cellular integrity.

Shaven and unshaven rats were exposed to a cold stress at 4 degrees C for 6 hr (SE and UE). Control animals remained at room temperature (SC and UC). Hypothermia was induced in group SE, with mean rectal temperature of 22.0 +/- 2.0 degrees C (+/- S.E.M.). All other groups were normothermic, had similar arterial pO2 and hepatic tryptophan oxygenase levels. Acute hypothermia induced a sloughing of cells from the villi into the lumen of the gut, as indicated by an increased DNA in luminal washings. However, there was an unimpaired 3H-thymidine incorporation into the DNA of the intestinal mucosal cells and those present in lumina washes. Intestinal disaccharidases and alkaline phosphatase were not altered. This suggests that more severe cellular alterations reported earlier in hypothermia may have been caused by associated factors other than a decreased body temperature.

Alkaline Phosphatase↗
PubMed1978

Effects of enteric microbial overgrowth on small intestinal ultrastructure in the rat.

The ultrastructural effects of bacterial proliferation in the upper gastrointestinal tract induced by intraperitoneal injections of mecamylamine HCl were investigated in rats. We found increased populations of nonspecific enteric bacteria in the lumen of the upper small intestine and ultrastructural abnormalities in the absorptive epithelial cells, including increased numbers of lysosomal vacular structures, fused microvilli and dilated endoplasmic reticulum. The bacteria did not penetrate into the damaged mucosal cells and so actual cytoplasmic infiltration is apparently not required in order to cause these ultrastructural changes. The alterations were not merely due to the pharmacologic agent we used, mecamylamine, since rats with subnormal numbers of enteric bacteria in the upper small intestine, whether subjected to the course of the drug or not, did not display the ultrastructural changes noted above. Concomitant with increased numbers of enteric bacteria in the small intestine, there were increased concentrations of deconjugated bile salts and decreased absorption of glucose. These findings are compatible with the following hypothetical sequence of pathogenesis: mecamylamine leads to intestinal stasis leads to bacterial overgrowth leads to deconjugation of the bile salts leads to ultrastructural alterations.

Animals↗
PubMed1977

Interaction between dietary carbohydrates and intestinal disaccharidases in experimental diarrhea.

The effects of carbohydrate intake on jejunal disaccharidases in rats with chronic mannitol-induced, osmotic diarrhea were studied. Weanling rats were force-fed 5 ml/100 g of body weight of water of 20% mannitol (w/v 1300 mOsm) daily for up to 14 days. Diets containing 70% of either starch, sucrose, glucose, or 20% lactose with 50% starch were fed ad libitum. Mannitol-fed rats had increased water intake and diarrhea. They gained weight, but less than controls. The levels of intestinal disaccharidases in mannitol-fed rats were related to dietary carbohydrate intake. Seven days of mannitol treatment led to lactase and sucrase deficiencies in rats fed starch whereas jejunal maltase and alkaline phosphatase were unchanged. Deficiencies in lactase and maltase but not in sucrase were induced when rats were fed a sucrose diet, while a decrease only in sucrase occurred in rats fed a lactose-starch diet. Rats with mannitol-induced diarrhea fed a glucose diet had reduced levels of all disaccharidases. The changes in intestinal disaccharidases were not associated with alterations in the number of epithelial cells or ultrastructural abnormalities. 3H-thymidine incorporation into DNA following 7 days of mannitol treatment was similar to water-fed controls. Absorptive epithelial cells were not damaged and the microvilli were normal in height and appearance. These data suggest that the levels of specific disaccharidases show and enhanced dependence upon the corresponding dietary substrates during diarrhea induced by an osmotic load.

Alkaline Phosphatase↗
PubMed1977

Ultrastructural cytochemical analysis of blastic transformation of chronic myelocytic leukemia.

Ultrastructural cytochemical changes occurring during the blast phase of chronic myelocytic leukemia (CML) are described. Normal developing promyelocytes contain myeloperoxidase (MPO) -positive rough endoplasmic reticulum, nuclear envelope, and Golgi apparatus. All secretory granules of normal promyelocytes are also MPO-positive. In this study we have found abnormal promyelocytes with MPO-positive as well as MPO-negative secretory granules in blast phase CML patients which contrast with the normal pattern of MPO distribution in most CML patients not in the blast phase or in nonleukemic controls. Alkaline phosphatase activity was found in the nuclear envelope of blasts and promyelocytes of one of the blast transformation patients who had a markedly increased leukocyte alkaline phosphatase score. The cytochemical changes in the distribution of MPO suggest that immature leukemic cells may alter their patterns of secretory granule production. Such processes may reflect the emergence of an abnormal clone of cells during the blastic transformation of CML.

Alkaline Phosphatase↗
PubMed1975

Circulation and turnover of synaptic vesicle membrane in cultured fetal mammalian spinal cord neurons.

Intact neurons in cultures of fetal rodent spinal cord explants show stimulation-dependent uptake of horseradish peroxidase (HRP) into many small vesicles and occasional tubules and multivesicular bodies (MVB) at presynaptic terminals. Presynaptic terminals were allowed to take up HRP during 1 h of strychnine-enhanced stimulation of synaptic transmitter release and then "chased" in tracer-free medium either with strychnine or with 10 mM Mg++ which depresses transmitter release. Tracer-containing vesicles are lost from terminals under both chase conditions; the loss is more rapid (4-8 h) with strychnine than with 10 mM Mg++ (8-16 h). There is a parallel decrease in the numbers of labeled MVB's at terminals. Loss of tracer with 10 mM Mg++ does not appear to be due to the membrane rearrangements (exocytosis coupled to endocytosis) that presumably lead to initial tracer uptake; terminals exposed to HRP and Mg++ for up to 16 h show little tracer uptake into vesicles. Nor is the decrease likely to the due to loss of HRP enzyme activity; HRP is very stable in solution. During the chases there is a striking accumulation of HRP in perikarya that is far more extensive in cultures initially exposed to tracer with strychnine than 10 mM Mg++ regardless of chase conditions. Much of the tracer ends up in large dense bodies. These findings suggest that synaptic vesicle membrane turnover involves retrograde axonal transport of membrane to neuronal perikarya for further processing, including lysosomal degradation. The more rapid (4-8 h) loss of tracer-containing vesicles with strychnine may reflect vesicle membrane reutilization for exocytosis.

Axons↗